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J. Biol. Chem., Vol. 280, Issue 2, 1678-1687, January 14, 2005

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Stimulus-specific Induction of a Novel Nuclear Factor-B Regulator, IB-, via Toll/Interleukin-1 Receptor Is Mediated by mRNA Stabilization^*

Soh Yamazaki, Tatsushi Muta¶, Susumu Matsuo, and Koichiro Takeshige

From the Department of Molecular and Cellular Biochemistry, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582 and Host and Defense, PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan

We have recently identified an inducible nuclear factor-B (NF-B) regulator, IB-, which is induced by microbial ligands for Toll-like receptors such as lipopolysaccharide and the proinflammatory cytokine interleukin (IL)-1 but not by tumor necrosis factor (TNF)-. In the present study, we examined mechanisms for stimulus-specific induction of IB-. The analysis of the IB- promoter revealed an essential role for an NF-B binding sequence in transcriptional activation. The activation, however, did not account for the Toll-like receptor/IL-1 receptor-specific induction of IB-, because the promoter analysis and nuclear run-on analysis indicated that its transcription was similarly induced by TNF-. To examine post-transcriptional regulation, we analyzed the decay of IB- mRNA, and we found that it was specifically stabilized by lipopolysaccharide or IL-1 but not by TNF-. Furthermore, we found that costimulation with TNF- and another proinflammatory cytokine, IL-17, elicited the IB- induction. Stimulation with IL-17 alone did not induce IB- but stabilized its mRNA. Therefore, IB- induction requires both NF-B activation and stimulus-specific stabilization of its mRNA. Because IB- is essential for expression of a subset of NF-B target genes, the stimulus-specific induction of IB- may be of great significance in regulation of inflammatory reactions.

Received for publication, August 31, 2004 , and in revised form, November 1, 2004.

The nucleotide sequence(s) reported in this paper has been submitted to the DDBJ/GenBank^TM/EBI Data Bank with accession number(s) AB074898.

^* This work was supported in part by grants-in-aid for scientific research from the Ministry of Education, Science, Sports, and Culture of Japan (to S. Y., T. M., and K. T.) and grants from the Kao Foundation for Arts and Sciences (to S. Y.), the Naito Foundation (to T. M.), and the Kaibara Foundation (to T. M.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ To whom correspondence should be addressed. Tel./Fax: 81-92-642-6103; E-mail: tmuta{at}mailserver.med.kyushu-u.ac.jp.

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